Herpes simplex keratitis is the most prevalent severe ocular infection in this country. The propensity of this infection to recur throughout life and to produce irreversible structrual alterations of the cornea and intraocular structures results in considerable visual morbidity, medical expense, and loss of productivity of otherwise healthy individuals. Currently effective therapy of herpes simplex keratitis is directed only at control of the replicating virus in the cornea. There is no method for blocking access of the virus to the latency site, or preventing recurrent shedding of virus and consequent herpetic keratitis. The key to control of this debilitating disease appears to be the knowledge of the mechanism of recurrent herpes. It has been recently determined that passage of current through the trigeminal nerve of the rabbit elicits rapid release of virus at the eye. The response appears to be dose related. Application of this system to the rabbit ocular model has the potential of manifying the reactivation process to levels commensurate with sensitivity of available probes such as the highly purified specific antisera to early virus coded polypeptides and the methods of quantitative culture of virus inspected cells. Identification and subsequent study (ultstructural) of neurons containing antigens suggestive of early viral activity should enhance our knowledge of the mechanism of reactivation. In addition, this system for multiple viral inductions provides a means of investigating whether episodes of recurrent ocular herpes are self-perpetuating and whether this can be manipulated by either drug therapy or post immune factors.